Ramon Dillon Perez

B.A, 2015, New York University, New York, NY
Advisor: Erich Mackow
Email: Ramon.D.Perez@stonybrook.edu

Research Interests

Hantaviruses (HVs) are negative stranded RNA viruses with a tri-segmented genome and the only member of the Bunyaviridae family that is transmitted to humans by small mammals. In the Americas, HVs cause HV pulmonary syndrome (HPS) a highly lethal acute pulmonary edema. Andes virus (ANDV) causes HPS and is the only HV is spread person to person and able to cause highly lethal pulmonary edema in an animal model. Despite successful reverse genetics for other bunyaviruses, similar approaches to generate HVs from recombinant S, M and L plasmids have failed and limit our ability to develop attenuated HV vaccines. My interest in the Mackow lab is to investigate novel functions of the ANDV polymerase as a means of defining attenuation mechanisms and developing reverse genetics. The HV Pol protein is an RNA Dependent RNA Polymerase (RdRP, Pol, 220 kDa.) with RNA transcriptase, replicase and helicase activities. The N-terminal 200 residues of Pol also contains an endonuclease (Endo) that cleaves viral and cellular RNAs. Mutations in the Endo domain (K44A and others) permit Pol protein to be detected and demonstrate the novel autocatalytic suppression of Pol expression that restricts viral replication and fosters viral persistence. Encoded Endo functions presumably direct novel cytoplasmic cap-snatching that primes hantavirus mRNA synthesis. Pol directed cap-snatching fit potential cytoplasmic mRNA/miRNA processing body (pBody) functions, although details of Pol function, localization and cap-snatching are poorly defined. I am interested in analyzing Pol and Endo domain K44A mutant interactions with pBody proteins and determine if expressing helper K44A Pol proteins in trans permits development of HV reverse genetics.
 

McIntosh, M.T., Koganti, S., Boatwright, J.L., Li, X., Spadaro, S.V., Brantly, A.C., Ayers, J.B., Perez, R.D., Burton, E.M., Burgula, S., MacCarthy, T., and Bhaduri-McIntosh, S. (2020). STAT3 imparts BRCAness by impairing homologous recombination repair in Epstein-Barr virus-transformed B lymphocytes. PLoS Pathogens 16(10).e1008849.

Xu, H., Perez, R.D., Frey, T.R., Burton, E.M., Mannemuddhu, S., Haley, J.D., McIntosh, M.T., and Bhaduri-McIntosh, S. (2019). Novel replisome-associated proteins at cellular replication forks in EBV-transformed B lymphocytes. PLoS Pathogens doi.org/10.1731/journal.ppat.1008228.